Bryostatin-1 improves function in arteries with suppressed endothelial cell autophagy.

Jae Min Cho, Seul-Ki Park, Sohom Mookherjee, Emily Carolyn Peters, Paulo W Pires, J David Symons

Department of Nutrition and Integrative Physiology, Division of Endocrinology, Metabolism and Diabetes, and Program in Molecular Medicine, University of Utah, Salt Lake City, UT, USA. [email protected]. · pubmed

Paper

Abstract

We have previously reported that when autophagy is suppressed in endothelial cells (ECs), a glycolytic defect limits shear-stress -induced ATP production to an extent that purinergic 2Y1 receptor (P2Y1R)-mediated activation of EC nitric oxide (NO) synthase (eNOS) is compromised. Subsequently we demonstrated the functional relevance of this finding in arteries from mice with genetic, pharmacological, and age-associated EC autophagy impairment. Using gain and loss of function approaches in vitro, we further revealed that p-PKCδ

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Research summary

Bryostatin-1 enhances endothelial cell function by mitigating the effects of suppressed autophagy. The study addresses a mechanism related to endothelial dysfunction, which is a significant factor in age-related vascular diseases, thus contributing to the understanding of aging processes.

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